Hello Emmel. The case is very interesting and with very points ofdiscussion:First, in our ICU rarely we use actually PA catheter,so, estimated EDP is made by echo...with multimodal approach.Weuse dinamic predictors of fluid responsiveness like delta pulsepressure, delta SV, delta IVC diameter and not static index like CVPor Wedge Pressure.We use thoracic echo to look if patients haveUS B lines, expression (not always) of elevated evLW and indicative oflung edema.Yes we use diuretics in case when ventricularinterdependence occurs or likely occurs, US B lines are present orbiventricular disfunction appear and always when is clear thatpatients are not fluid responsive. The point here is a titrated usebecause risk of hipovolemia and if this happens, yes, cardiac outputdrops.If PH have a postcapillary component restoration of LVfunction and maybe diuretics still may be considered.Thinking inthis patient the RV maybe improve with supportive care and treatingthe infection. Miocardial stunning postCPR is another possibility. So,dobutamine is the inotropic of choice, simple because the afterload ofRV drops with it.

Hello Pablo!Thanks a lot for comment!This case was a"desaster".That patient had a severe COPD and actually an acuteinfection- exacerbation (gram-negative rod-cells). mechanicalventilation was very hard, but we could avoid hypoxaemia.You´redefinitely right: volume is the wrong way. Using echocardiography wetried a short volume-challenge with 250ml cristaloid-infusion: noeffect on haemodynamic (blood-pressure, estimated stoke-volume). But Idon´t agree with loop-diuretics in that situation: CVP was 17 mmHgand echocardiographic estimated LVEDP was 19 mmHg and I think thatpatient needs that preload for the left ventricle in this case (highdose catecholamines, about 75ml/h spontaneous diuresis). Do you haveanother experience in cases like this especially with diuretics?Definitely no lung oedema! So please let me know, I´m very interestedin your experiences! Maybe glyteroltrinitrate could help if one wantsto lower LVEDP and PVR.The patient had definitely no pulmonaryembolism (ct-scan, TEE). But he had two components of PH:post-capillary PH and a remodeling of pulmonary arteries (TPG > 15mmHg; PVR > 250 dyn+sec+cm^-5 in echocardiographic estimation). Afterall it is a severe seconary PH in context of severe COPD incombination with ischemic component (condition after cardiacinfarction of inferior wall caused by occlusion of RCA for years)./>Last cardiac catheter was 2 weeks before admission to our icu: thereis no possibility to improve the coronary status. We decided againstcardiac catheter.We started application ofphosphodiesterase-inhibitor type 5 (revatio 3 x 20 mg/d). No iloprostin that situation because in bronchoscopy we found in all bronchia alot of pus and I think in that situation there won´t be nobenefit.Best wishes and thanks a lot for your opinion!I´mglad that you join EchoJournal.Jörg.

about 85 y old patient with severe acute RV-failure in context of chronic ischemic RV-failure. No sign of pulmonary embolism in initial TEE and ct-scan. First TTE we found a distinct RV-wall movement disorder. haemodynamic deteriorated rapidly, so we had to start cardiac resusciation for 3 minutes. in TTE we could see a distinct rv-pressure-overload with systolic d-sign. Actually vasopressor and inotropics save the situation. Any other hints in treatment of acute RV-Failure except inotropics and/ or vasopressor?